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Background: Cardiovascular diseases (CVD) account for approximately 50% of the total deaths in Turkey. Most of them are related with atherosclerotic coronary heart disease. Predictive value of endothelial dysfunction markers related with the earliest stage of atherosclerosis has been getting more attention. We hypothesized that differences in endothelial dysfunction biochemical markers among genders would aid to capture proatherogenic activity that was not diagnosed by conventional risk assessment scoring systems. Methods: We assessed the endothelial dysfuntion markers in 92 Turkish adults who were in the "low CV risk group" according to ESC (European Society of Cardiology)-Score Risk Charts. We compared the males and females. Results: We observed higher endothelial dysfunction rates in males, with higher median and mean levels of e-NOS, ox-LDL before and after adjustment for HDL lowness and obesity (P = 0 .0 1 8, P = 0.036 for NOS; P = 0 .000 , P= 0.004 for ox-LDL, respectively). Men had higher hsCRP levels than females before adjustment (P = 0.021). Decreased e-NOS levels were related with FMD for females before adjustment for confounders (P = 0 .0 28). We also found significant correlation between e-NOS and ox-LDL levels both before (r= 0.360, P< 0.001) and after adjustment (r= 0.366, P< 0.01) for confounders which pointed out the nitrosative stress. In multivariate regression analyses, after adjusting for other endothelial dysfunction markers which were not included in the ESC-risk scoring system, decreased e-NOS levels were independently asssociated with impaired flow mediated dilatation for females (odds ratio 0.3; P= 0.038). Conclusions: Our results underline the importance of gender in evaluating endothelial dysfunction biochemical markers to assess cardiovascular risk for low CV risk indivuals.

Abstract Background In experimentally induced puromycine aminonucleoside nephrosis (PAN) animal models, nephrotic syndrome with minimal change disease and focal and segmental sclerosis-like nephritis similar to that in human is demonstrated; however, the real mechanism of PAN is not yet elucidated. Platelet derived endothelial cell growth factor (PD-ECGF), an endothelial mitogen protein, is believed to take part in microvessel formation and in stimulation of angiogenesis and its expression has not been totally demonstrated in PAN rats yet. In this study, we aimed to examine PD-ECGF expression in acute and chronic PAN induced in rats and find out the association between its expression and the stages of angiogenesis in kidney. Methods For the experiment, twenty-four Male Wistar Albino rats were used and divided into four groups; control group (n = 6), pre-proteinuria group (n = 6), acute group (n = 6) and chronic group (n = 6). We compared statistically all data by One-way ANOVA Test followed by Dunn Multiple Comparison Test. Results Proteinurea levels in control and pre-proteinuria groups were not statistically different; however, it was remarkably higher in the acute nephrosis group and significantly greater in the chronic nephrosis group than control group (p < 0.0025). In pre-proteinuria group, the serum albumin and creatinine clearances also did not significantly differ from the control group. On the other hand, in the acute and chronic nephrosis groups, serum albumin and creatinine clearances progressively decreased (p < 0.05). In our immunohistochemical studies, we showed elevated PD-ECGF expression in glomeruli of acute and chronic PAN rats. Microscopic and ultrastructural appearances of the glomeruli of acute and chronic PAN showed various sequential steps of angiogenesis, macrophages and immature capillaries with primitive lumens and apoptotic endothelial cells in the increased mesangial matrix. Conclusions It is reported that acute and chronic PAN progressively increase PD-ECGF expression and following induction of angiogenesis in the affected glomeruli.

Objective: The study tested whether cardiovascular corresponding LPA risk genotypes improve pre-eclampsia and coronary heart disease (CHD) risk prediction beyond conventional risk factors.Background: Studies have shown that women specific risk factors for cardiovascular disease (CVD) have taken an attention recently. It might be possible to identify women who have the highest risk in developing CVD in their further lives. It is well-known that Lp(a) levels have an impact on increased risk of CVD which is affected by LPA gene. Further, LPA risk genotypes are not considered in cardiovascular risk prediction.Methods: We have included 200 pregnant Turkish women into the study. We stratified the preeclamptic (PE) group: early (EOP) (28.7 ± 3.0 weeks) and late onset (LOP) (36.0 ± 1.4 weeks). 14 LPA SNPs were evaluated in the study. Rs9355296 and rs3798220 were found as independent risk factors for preeclampsia by logistic regression analysis. A positive correlation was found between rs9355296 and the diagnostic criteria of preeclampsia. Further rs9355296 G/* carriers have higher vascular inflammation rather than AA carriers.Conclusions: The findings reveal that LPA genetic variability with high inflammatory response might be an indication of future cardiovascular events. [ABSTRACT FROM AUTHOR]

Background: Cardiovascular disease is the leading cause of death in the world and is associated with significant morbidity. Atherosclerosis is the main cause of cardiovascular disease (CVD), including myocardial infarction (MI), heart failure, and stroke. The mechanism of atherosclerosis has not been well investigated in different aspects, such as the relationship between oxidative stress and endothelial function. This project aims to investigate whether an oxidative enzyme vascular peroxidase 1 (VPO1) and activating transcription factor 4 (ATF4) can be used as biomarkers in highlighting the pathogenesis of the disease and in evaluating the prognosis of the relationship with endoplasmic reticulum and oxidative stress. This paper used artificial neural network analysis to predict cardiovascular disease risk based on new generation biochemical markers that combine vascular inflammation, oxidative and endoplasmic reticulum stress. Methods: For this purpose, 80 patients were evaluated according to the coronary angiography results. hs-CRP, lipid parameters and demographic characteristics, VPO1, ATF4 and Glutathione peroxidase 1(GPx1) levels were measured. Results: We found an increase in VPO1 and hs-CRP levels in single-vessel disease as compared to controls. On the contrary, ATF4 and GPx1 levels were decreased in the same group, which was not significant. Our results showed a significant positive correlation between ATF4 and lipid parameters. A statistically significant positive correlation was also observed for VPO1 and ATF4 (r=0.367, P